Parkinson's Disease

What is Parkinson’s Disease?

Parkinson's disease (PD) is a chronic, neurodegenerative disease that primarily affects movement. The cause of PD is unknown, and although there is presently no cure, there are treatment options including medication and surgery to manage its symptoms. An estimated 500,000 to 1 million people in the US are living with Parkinson's disease and the National Institute of Neurological Disorders and Stroke (NINDS) estimates that Parkinson’s disease carries an annual cost of over $5.6 billion to our society.

Symptoms of Parkinson's disease include:

Tremor (shaking) - begins in hands and/or fingers of one limb

Pill-rolling tremor - rubbing of the thumb and forefinger

Slowed movements - reduction in ability to move

Shuffling gait - dragging of feet when walking

Muscle stiffness - limits range of motion and causes pain

Speech changes - slurred words and low speech volume

Writing changes - illegible handwriting

Stooped posture and balance problems

Fatigue - may precede motor symptoms

Excessive daytime sleepiness (EDS) - including sudden "sleep attacks"

How is Parkinson’s Disease Linked to Mitochondrial Dysfunction?

Parkinson's disease results from a deterioration of the neurons (nerve cells) in the region of the brain called the substantia nigra. These neurons normally produce the neurotransmitter dopamine that sends signals to the basal ganglia, a mass of nerve fibers that helps initiate and control patterns of movement. Dopamine functions in the brain as an inhibitor of nerve impulses and is involved in suppressing unintended movement. When dopamine-producing (dopaminergic) neurons are damaged or destroyed, dopamine levels drop and the normal signaling system is disrupted. In both primary and secondary parkinsonism, the physiological effects of this deterioration do not manifest until roughly 60 to 80 percent of dopaminergic neurons are destroyed.

Evidence suggests that mitochondria play a central role in ageing-related neurodegenerative diseases. Mitochondria are critical regulators of cell death, a key feature of neurodegeneration. It is a known fact that when the energy generating capacity of a cell falls below a critical threshold the cell enters into a process known as “apoptosis” or programmed cell death. Once a substantial number of cells in the substantia nigra die off, symptoms of PD will begin to appear.

Mutations in mitochondrial DNA and oxidative stress both contribute to ageing, which is the greatest risk factor for neurodegenerative diseases. In all major examples of these diseases there is strong evidence that mitochondrial dysfunction occurs early and acts causally in disease pathogenesis.

Mutations to mitochondria can occur through exposure to environmental toxins, such as medications or pesticides, or they can occur as a result of genetics – both inherited and acquired mutations.